These hemiplegic attacks can cause anything from mild weakness to complete paralysis on one or both sides of the body, and they can vary greatly in duration.

Besides hemiplegia, symptoms of the disorder include an extremely broad range of neurological and developmental impairments which are not well understood.

Non-paroxysmal symptoms tend to be side effects of AHC which are present at all times, not just during episodes or attacks.

One of the unique characteristics of AHC is that hemiplegic attacks, as well as other symptoms which may co-occur with hemiplegia, cease immediately upon sleep.

[4][6][7] Paralysis is also often accompanied by changes in skin color and temperature, sweating, restlessness, tremor, screaming, and the appearance of pain.

AHC is not exclusively limited to childhood – attacks in some cases become milder after the first ten years of life, but they never completely disappear.

[4] A final symptom that may be considered paroxysmal is a temporary change in behavior - some patients will become unreasonable, demanding, and aggressive either before or after an attack.

[4][8] Overall however, EEG during episodes and other investigative methods such as brain MRI, TACs, angiographic MRIs and CFS have normal results.

[12] It is not known whether AHC is a progressive disease, but severe attacks are suspected to cause damage which results in permanent loss of function.

[7] 100% of children studied in the USA have had some form of mental impairment, which is usually described as mild to moderate,[4] but varies greatly among individuals.

[citation needed] Recent research suggests that AHC is caused by a de novo (spontaneous) genetic mutation in the ATP1A3 gene[13][14][2] on chromosome 19 (locus 19q13.31) which encodes enzyme ATP1A3.

[9] The disorder most closely related to AHC is familial hemiplegic migraine which is caused by a mutation in a gene for calcium channel receptors.

There are several generally accepted criteria which define this disorder, however other conditions with a similar presentation, such as HSV encephalitis, must first be ruled out.

The initial four criteria for classifying AHC were that it begins before 18 months of age, includes attacks of both hemiplegia on either side of the body, as well as other autonomic problems such as involuntary eye movement (episodic monocular nystagmus), improper eye alignment, choreoathetosis, and sustained muscle contractions (dystonia).

Diagnostic criteria were also expanded to include episodes of bilateral hemiplegia which shifted from one side of the body to the other.

These screening criteria include focal or unilateral paroxysmal dystonia in the first 6 months of life, as well as the possibility of flaccid hemiplegia either with or separate from these symptoms.

Paroxysmal ocular movements should also be considered, and these should include both binocular and monocular symptoms which show in the first 3 months of life.

[7] There is, however, not yet any conclusive evidence that AHC is fatal or that it shortens life expectancy, but the relatively recent discovery of the disorder makes large data for this type of information unavailable.

Common triggers include temperature changes, water exposure, bright lights, certain foods, emotional stress, and physical activity.

[citation needed] In 2009 through 2011 clinical research at the University of Utah investigated whether sodium oxybate, also known as gamma-hydroxybutyric acid is an effective treatment for AHC.